More Vitamin D and HDL

I’m seeing more and more of it and I am convinced that there is a relationship: significant boosts in HDL cholesterol from vitamin D supplementation.

To my knowledge this remains an undescribed and uncharacterized phenomenon. There have been several observers over the last two decades who have noticed that total cholesterol shows a seasonal fluctuation: cholesterol goes up in fall and winter, down in spring and summer; year in, year out. This phenomenon was unexplained but makes perfect sense if you factor in vitamin D fluctuations from sun exposure.

I have come across no other substantiating evidence about fluctuations of HDL. But I am convinced that I am seeing it. Replace vitamin D to a blood level of 50 ng/ml, and HDL goes up if it is low to begin with. If HDL is high to begin with, say, 63 mg/dl, it doesn’t seem to change.

But, say, starting HDL is 36 mg/dl. You take niacin, 1000 mg; reduce high-glycemic index foods like breakfast cereals, breads, cookies, bagels, and other processed carbohydrate foods; exercise four days a week; add a glass of red wine a day; even add 2 oz of dark chocolate. You shed 15 lbs towards your ideal weight. After 6 months, HDL: 46 mg/dl. Better but hardly great.

Add vitamin D at a dose of, say, 4000-6000 units per day (oil-based gelcap, of course!), and re-check HDL two or three months later: 65 mg/dl.

I’ve seen it happen over and over. It doens't occur in everybody but occurs with such frequency that it’s hard to ignore or attribute to something else. What I’m not clear about is whether this effect only occurs in the presence of the other strategies we use to raise HDL, a “facilitating” effect, or whether this is an independent benefit of HDL that would occur regardless of whatever else you do. Time will help clarify.

We are tracking our experience to see if it holds up, how, and to what degree on a more formal basis. Until then, a rising HDL is yet another reason—-among many!-—to be absolutely certain your 25-OH-vitamin D3 level is at 50 ng/ml or greater.

How high is an ideal vitamin D blood level? If 50 ng is good, is 60 or 70 ng even better? Probably not, but there are no data. We have to wait and see. Unlike a drug that enjoys plentiful “dose-response” data, there are no such observations for vitamin D into this higher, though still “physiologic,” range.

Thin ice

How long can an industry built on ignorance and deception continue its practices in the new Information Age?

I don’t think it can for long. I talk to hospital administrators who believe that their source of competition is the hospital across town, battling for the same patients. I speak to my colleagues, the cardiologists, who believe that the current model is sustainable—take every willing body to the catheterization laboratory or operating room for heart procedures, the revenue-generating engine of income and expanding heart programs.

I speak to primary care physicians, who are dumbfounded and perplexed and have no idea which way things are going. They are trapped in a peculiar position: most have signed contracts and are employees of the hospital. They are legally bound to support the cardiologists who take anybody possible to the catheterization laboratory or direct patients to other profit-making procedures.

Much of this system depends on the willingness of the participant, meaning you and the health care seeking public. What happens when the truth comes out and disseminates widely through the thinking populace? What happens to hospitals and physicians and the vast structures they’ve built when the bottom drops out for 50% of their “market?

The proverbial cow manure will hit the fan. Upheavals in the medical industry will rival the changes that the automobile or telephone brought early in the last century. Cardiologists, immense hospital heart programs, and the vast economic infrastructure they spawned will go the way of stage coach manufacturers and the telegraph.

What form will the broad exposure of detailed information in health take? I’m not sure, but it will certainly come. The collaborative efforts that created the Linux operating system and have challenged the monopoly of Microsoft Windows, or the emergence of the extraordinary Wikipedia as a repository of human knowledge that dwarfs the venerated Encylopedia Brittanica, will eventually overtake the American medical system, the heart disease industry in particular.

If you base your future on the welfare of your local hospital or the manufacturers of stents, operating room equipment for heart bypass, or similar industries, watch out. The ice is thin. And as the spring warms the air around you, it gets thinner.

The Track Your Plaque program is our first step in broadcasting the message of self-empowerment in heart health care and an attempt to wrestle control away from the profit-seeking forces that dominate. As we grow, we not only hope to broadcast the message more widely, but expand the message to other areas of health. I predict that the collaborative, let’s-all-pitch-in-and-help spirit of the Information Age, “version 2.0,” will spark the change.

Vitamin D and cancer

Although this is a Blog about heart scans and heart disease, I came across a helpful video from Dr. Joseph Mercola about vitamin D and cancer that's worth viewing. Though I do not agree with many of Dr. Mercola's on-the-edge views, he does come up with some good thoughts and, in this instance, a useful educational tool about vitamin D.

You can view his video (which he claims crashed his server, due to the excessive demand for downloads) by cutting and pasting the address into your URL bar (above):

http://v.mercola.com/blogs/public_blog/How-to-Reduce-Your-Risk-of-Cancer-By-50--8790.aspx

Also, for my many patients who I've directed to look in my Blog for Dr. Reinhold Vieth's webcast presentation on vitamin D, here's the address:

http://tinyurl.com/f93vl

Perhaps I carry on too much about vitamin D. But I've come to respect this "nutrient" as among the most powerful strategies I've seen for dramatically improving control over coronary plaque growth as well as other aspects of health, as Drs. Mercola and Vieth eloquently detail.

Lipoprotein(a), menopause, and andropause

Lipoprotein(a) is a curious lipoprotein. Not only is it a genetic pattern with numerous variations, it is also one that shows a predictable age-dependent rise.

Women in particular are prone to this effect, men to a lesser degree. As we age, many hormones recede, particularly growth hormone, testosterone, the estrogens (estradiol, estriol, estrone), progesterone, and DHEA, among others. This is not a disease but the process of senescence, or aging.

When we're young, estrogens, testosterone, and DHEA all exert suppressive effects to keep lipoprotein(a), Lp(a), at bay. But as a woman proceeds through her pre-menopausal and menopausal years, and as a male passes through his fourth decade, there is an accelerated decline of these hormones. As a result, Lp(a) crawls out of its cave and starts to sniff around.

Typically, a woman might have a Lp(a) of 75 nmol/l (approximately 30 mg/dl) at age 38. Ten years later, at age 48, her Lp(a) might be 125 nmol/l (app. 50 mg/dl), all due to the decline of estrogens and DHEA. A parallel situation develops in males due to the drop in testosterone. For this reason, it may be necessary to re-check Lp(a) once after the fourth decade of life if you've had a level checked in your younger years.

This opens up some interesting therapeutic possibilities. If receding hormones are responsible for unleashing Lp(a), hormones can be replenished to reduce it. In males, this is relatively straightforward: supplement human testosterone and Lp(a) drops about 25%.

In women, however, it's a bit murkier, thanks to the negative experince reported using horse estrogens (AKA Premarin) in the HERS Trial and Women's Health Initiative. You'll recall that women who take horse estrogens and progestins (synthetic progesterone) do not experience less heart attack and develop a slightly increased risk of endometrial and breast cancer. There was, however, a poorly-publicized sub-study that showed that women with Lp(a) experience up to 50% fewer heart attacks on the horse/synthetic combination.

Wouldn't it be nice to have a large trial examining the safety/advisability of human estrogens and progesterone? To my knowledge, no such confident study in a significant number of women exists, since there's so little money to be made with human hormonal preparations.

For these reasons, we use lots of DHEA, generally at doses of 25 to 50 mg per day. It makes most people feel good, boosts energy modestly, increases muscle, and reduces Lp(a) up to 18% in women, a lesser quantity in men.

"I have never seen regression"

At a presentation at the American College of Cardiology meetings in New Orleans yesterday (March 27, 2007), Dr. Arthur Agatston declared "I have been doing CT for many years, and I have never seen regression."

Whooooaaaa. Wait a minute here. I have great respect for the work Dr. Agatston has done over the years. He is, after the originator of the scoring algorithm that allows us to score CT heart scans (though a more accurate measure, the volumetric score, is the one we often use behind closed doors because of modestly increased accuracy and reproducibility). His diet program, the South Beach Diet, has achieved enormous success and is indeed an effective approach for both weight loss and correction of many weight-related causes of heart disease.

But he has never seen regression? Why would this be when we see it all the time? When we see heart scan scores drop 30%, it's hard to believe that with some savvy he has never seen regression (drop in score).

I can only attribute the difference to the more intensive endpoints we advocate (e.g., 60-60-60 for lipid values); the incorporation of adjuncts like fish oil, vitamin D, l-arginine; attention to non-cholesterol issues and intensified treatments for each. I doubt that the populations we see differ substantially.

As much as I admire Dr. Agatston's accomplishments, I believe that he is behind the times on this issue. No regression is so starkly different from the Track Your Plaque experience. I believe that relying only on statin drugs and diet will slow but will not stop plaque growth. It will also rarely, if ever, drop your score.

Attention to detail and a little insight into better preventive strategies really pays off. While not everyone in the Track Your Plaque experience will drop their score, a substantial number do. Many more slow plaque growth dramatically. And, as time goes on, our track record gets stronger and stronger.

COURAGE to do better

The results of the long-awaited COURAGE Trial were announced today at the American College of Cardiology meetings in New Orleans.

In this trial, 2200 participants with stable coronary disease (i.e., not unstable, in which heart attack or death is imminent) were randomly assigned ("randomized") to either angioplassty/stent or "maximal medical therapy." Medical therapy means such things as aspirin, beta blocker drugs, and statin cholesterol drugs. There was virtually no difference between the groups in rate of heart attack and death from heart disease over a period of up to 7 years.

These results have caused a stir in the media and my colleagues, trying to sort out of the implications. However, I think there's one observation in particular worth making for those of us who tend to scoff at the conventional approach to coronary disease. That is, 1 of 5 people had a heart attack or died from heart disease in both groups. That's a lot. Even more ended up with a procedure (angioplasty, stent, or bypass). In other words, the "maximal medical therapy" instituted in participants was hardly a success. Though angioplasty and stenting failed to prove superiority, both really stunk. Both permitted a lot of catastrophes to occur.

"Maximal medical therapy," in other words, is a laughable concept. It doesn't include raising HDL, suppressing small LDL, reducing Lipoprotein(a), addressing inflammatory issues. It does not include omega-3 fatty acids from fish oil, nor does it address the severe degrees of vitamin D deficiency that are proving, in the Track Your Plaque experience, to be among the most potent causes of atherosclerotic plaque known. It includes a sad attempt at diet, as advocated by the American Heart Association, a diet that, in my view, causes heart disease and is distorted by the powerful political and financial influence of food manufacturers.

If the trial were to be done again, I'd like to see the "maximal medical therapy" arm be represented by a more effective program like the Track Your Plaque approach.

Value of a zero heart scan score

Margaret is 73. She's a very good 73. She loves children and works full-time in a daycare. She manages her own household, goes to dinner at least once each week with one or more of her adult children. She is slender and has never been in the hospital--until she developed an abnormal heart rhythm called atrial fibrillation.

Most people who develop atrial fibrillation do so with no immediate identifiable cause. However, Margaret has been a widow since her husband died 15 years ago of a heart attack. She was therefore especially frightened of any heart issues in her own health. Her doctor also raised the question of whether atrial fibrillation might represent the first hint of future heart attack.

So we advised a CT heart scan. Score: zero, or no detectable plaque whatsoever. This put Margaret's risk for heart attack as close to zero as humanly possible. (Nobody is truly at zero risk for heart attack for a number of reasons. One reason is that people do irrational things like take cocaine or amphetamines, or they take too much decongestant medication, all of which can trigger heart attack.)

The heart scan settled it. Margaret has the sort of atrial fibrillation which likely simply develops as a result of "wear and tear" on the heart's electrical impulse conducting system and it has nothing to do with coronary heart disease or heart attack.

As that MasterCard commercial goes: Cost of a heart scan: About $200. Peace of mind: priceless.

You're at the cutting edge

If you're a participant in the Track Your Plaque program for atherosclerotic plaque regression, you are at the cutting edge of health.

Few physicians give this issue any thought. Chances are, for instance, that if you were to bring up the subject of reversal of heart disease to your primary care physician, you'd get a dismissive "it's not possible," or " Yeah, it's possible but it's rare."

Ask a cardiologist and you might make a little more progress. He/she might tell you that Lipitor 80 mg per day or Crestor 40 mg per day might achieve a halt in plaque growth or a modest reduction of up to 5-6%. If they've tried this strategy, they would likely also tell you that hardly anybody can tolerate these doses for long due to muscle aches. I'd estimate that 1 of 10 of my colleagues would even be aware of these studies.

Both groups are, however, reasonably adept at diagnosing chest pain, an everyday occurrence in hospitals and offices. Chest pain, for them, is a whole lot more interesting. It holds the promise of acute catastrophe and all its excitement. It also holds the key to lots of hospital revenues. Did you know that 80% of all internal medicine physicians are now employees of hospitals? They're also commonly paid on an incentive basis. More revenues, more money.

Ask Drs. Dean Ornish or Caldwell Esselstyn about reversal of heart disease and they will tell you that a very low-fat diet (<10% of calories)can do it. That's true if you use a flawed test of coronary disease like heart catheterization (angiograms) or nuclear stress tests (Ornish calls them "SPECT"). It would be like judging the health of the plumbing in your house by the volume of water flowing out the spigot. It flows even when the pipes are loaded with rust.

In the Track Your Plaque experience, extreme low-fat diets (i.e., high wheat, corn, and rice diets) grotesquely exagerrate the small LDL particle size pattern, among the most potent triggers for coronary plaque growth. This approach also makes your abdomen get fatter and fatter and inches you closer to diabetes. Triglycerides go up, inflammation increases.

If you were able to measure the rust in the pipes, that would be a superior test. You can measure the "rust" in your "pipes," the atherosclerotic plaque in your coronary arteries, using two methods: CT heart scans or intracoronary ultrasound. Take your pick. I'd choose a heart scan. It's safe, accurate, inexpensive. I've performed many intracoronary ultrasounds for people in the midst of heart attacks or some other reason to go to the catheterization laboratory. But for well people, without symptoms, who are interested in identifying and tracking plaque? That's the place for heart scans.

In our program, 18-30% reductions in heart scan scores are common.

A stent--just in case

Burt came to me last week. He'd received a stent a few months earlier. He'd been feeling fine except for some fatigue. A nuclear stress test proved equivocal, with the question of an abnormal area of blood flow in the bottom (inferior wall) of the heart.

"The doctor said I had a 50% blockage. Even though it wasn't really severe, he said I'd be better off with a stent, just in case."

Just in case what? What justification could there be for implanting a stent "just in case"? (The artery that was stented did not correspond to the area of questionable poor blood flow on the nuclear stress test.)

Just in case of heart attack? If that's the case, what about the several 20 and 30% blockages Burt showed in other arteries? The cardiologist was apparently trying to prevent the plaque "rupture" that results in heart attack by covering it with a stent. Why stent just one when there were at least 7 other plaques with potential for rupture?

That's the problem. And that's why stents do not prevent heart attack (unless the stent is implanted in the midst of heart attack, when the rupturing plaque declares itself.) Of course, when no plaque is in the midst of rupturing, as with Burt, there's no way to predict which plaque will do so in future. Since only one plaque was stented, there is a 7 out of 8 chance (87.5%) that the wrong plaque was chosen. And that's assuming that there aren't plaques not detected by catheterization angiogram; there commonly are. The odds that the right plaque was chosen would be even lower.

In other words, stenting one blockage that is slightly more "severely blocked" in the hopes of preventing heart attack is folly. If it's not resulting in symptoms and blood flow is not clearly reduced, a stent can not be used to prevent plaque rupture. A stent is not a device to be used prophylactically. It is especially silly when an approach like ours is followed, since plague progession is a stoppable process.

Note: This issue is distinct from the one in which symptoms and/or an abnormal stress test show clearly reduced blood flow and flow is restored by implantation of a stent. While some controversies exist here, as well, a stent implanted under these circumstances may indeed provide some benefit.

How will you know your score dropped?

This issue came up twice this week.

Bill is a busy accountant. Two years ago, just after the tumult of the 2005 tax season was over, he got a CT heart scan. His score: 398. At age 53, this was a significant score. His internist did the usual: prescribed a statin (Zocor), told him to cut the fat in his diet, and be sure to exercise. (Yawn.)

Since then, Bill quit preparing tax returns and migrated to a less harried job in corporate accounting. It took two years since his heart scan for Bill to start thinking that perhaps his doctor's advice wasn't enough. If it was, he realized, everyone on a statin drug who made these minimal lifestyle changes would be cured of heart attack risk. Clearly not the case.

So Bill enrolled in the Track Your Plaque program. Our first step: Get another heart scan.

Bill was surprised. "Why another scan? I already had one!"

I explained to Bill that atherosclerotic plaque is like money: it grows in percentages, just like money in a bank account or in a mutual fund. If, for instance, you deposit $500 in a mutual fund and it yields 5% return, then after one year you will have $550. One year later, you will have 5% x $550, or $605. Another year: $665. In other words, growth is not 10% of the original amount you deposited. Growth is compounded, year over year. That's why money, when compounded, can grow so quickly.

Atherosclerotic plaque and your CT heart scan score do the same thing: they grow by a percentage of the current plaque quantity. In fact, we use the compound interest equation to calculate the annualized rate of plaque growth. But plaque grows at the extraordinary rate of 30% per year, on average. Imagine that was the rate of return on your money. You'd be the richest man or woman on earth.

Back to Bill. Now Bill, in his defense, was on a statin drug and did make modest efforts towards a (mis-guided) low-fat diet and walking four days per week. If, on a second CT heart scan, his score was:

398--No change. That's a success, since the expected rate of increase of 30% has been stopped. However, on his current program, this is highly unlikely. (I've seen it happen just once ever out of about 2000 people.)

250--Pop the cork on your champagne, because Bill needs to celebrate. He has substantially reversed his plaque. Highly unlikely on the current effort.

525 --The score is higher by 30%, so it has slowed, but it surely hasn't stopped. This is the most typical result on the sort of program Bill is following.

The message: Don't delay after your first heart scan score. It plaque grows like money with a huge return, there's no time like the present to take the steps to regain control.

Report from Washington II

Today's discussions at the Society for Cardiovascular Computed Tomography (SCCT) focused on atherosclerotic "plaque characterization".

As CT scanners get better and better at imaging the various components of plaque, some fascinating issues emerge:

--CT heart scans provide insights into what exactly is contained in an individual's atherosclerotic plaque that are not often provided even during heart catheterization. In other words, CT heart scanning is, in many instances, superior to heart catheterization, since it provides images of the artery wall, not just the internal contents.

--Progression (i.e., increase) in heart scan score is a powerful predicter of heart attack risk. Dr. Matthew Budoff of UCLA argued persuasively that the annual rate of increase in score is probably the most accurate measure of risk available, superior to cholesterol and calculated measures like the Framingham risk score.

--Coronary calcium scoring remains the best method to gauge total plaque throughout the entire coronary tree. In a person free of symptoms, the risk of a cardiac "event" (heart attack, death, procedures) is low and additional imaging (like CT angiography) is generally unnecessary.


Dr. Budoff, among the true thought leaders in CT heart scanning, also recounted his perspective on the history of heart scans. He noted that the questions asked through the years have evolved:




1995-2000 Should we do coronary calcium scans?

2000-2002 Do high or low risk patients benefit from coronary calcium scoring?

2003-2004 What is the better scanner, EBT or MDCT?

2006 How often should we perform coronary calcium imaging?


I believe that Dr. Budoff summarizes wonderfully where the Track Your Plaque programs fits into the overall scheme of things: Serial (repeated)CT heart scans to gauge progression or reversal is the wave of the future. We shouldn't just be interested in identifying persons at risk for heart attack. We should also be interested in showing the person at risk exactly how to reduce or eliminate that risk.

Report from Washington





I'm presently attending the Society for Cardiovascular Computed Tomography meetings in Washington, DC, along with 500 of my colleagues. It's exciting to see how interest in CT scanning for heart disease has balloonned in the past couple of years.

Several trends are noticeable today, based on the content and tone of the discussions:

--CT scanning of the heart, and imaging in general, is just getting started. In other words, the capabilities for CT scanners and other devices to detect heart disease (coronary and otherwise) are where the gasoline engine was in the 19th century. Scanning is getting faster, easier, safer, and more precise. Just as few people in 1905 could have predicted that automobiles would be computer-enhanced, high-speed, ubiquitous devices with several per household, the potential for CT imaging for heart disease is truly in its infancy.

--CT coronary angiography (so-called "64-slice CT scans") are not screening tests for hidden coronary disease in people without symptoms. I was grateful that this point has been made and reiterated by several speakers, as this is consistent with our views. Simple CT heart scans for coronary calcium scoring, in contrast, are screening tests. When the radiation exposure of CT angiograms are reduced to tolerable levels, then they may be used as screening tests. We are probably 3-4 years away from this point.

--Both stress testing and heart catheterizations will be partially replaced by CT scanning. In particular, over the next decade, you will see a dramatic drop in unnecessary catheterizations, i.e,, far less people saying "I had a heart cath but they told me that it was normal."


There has been heavy focus on applications of CT scanning for acute settings, particularly the emergency room and hospitals.

What has surprised me is that there is virtually no conversation whatsoever about the preventive uses of CT heart scanning. So far, only Dr. Daniel Berman of UCLA has shown that he has "seen the light": CT scans are a crucial tool for identification of early coronary plaque, and this tells us whether prevention is necessary and with what intensity.

There has been, however, no discussion at all about quantification of plaque in a program of reversal. Perhaps that should come as no surprise, given the imaging-technology focus of this convention. For most of my colleagues, prevention is also not terribly interesting. Identification and treatment of acute disease like impending heart attack is.

Of course, applying the information from your CT heart scan to empower you in a program and reversal is what the Track Your Plaque program is all about. I hope you see the light. I admit that it's not always easy to follow what we are advocating here. Perhaps not too different than telling someone in his horse-drawn buggy that one day he'll be driving a sleek car with onboard computerized mapping, air-conditioning, and micro-chips to modulate engine performance. He's probably tell us we're nuts.

I'll continue to update if any news relevant to our interests crops up in these meetings.

What about the Track Your Plaque failures?

I’d love to tell you that the Track Your Plaque program track record is of 100% success. It’s not.

It is very successful. But we’ve had some people who have failed and failed BIG. These are the people who've undergone bypass surgery, received one or more stents, or had heart attacks. Lesser failures are the people who’ve had large, undesirable increases in heart scan scores of >30% in one year. (The expected rate of increase in your heart scan score without preventive efforts is 30% per year, on average.)

What can we learn from those failures? There were several characteristics that stand out among this small group:

· Non-compliance--meaning they just didn’t stick with it. They started out right but then rapidly lost interest in maintaining all the pieces of the program and neglected their fish oil, niacin, gain weight, etc. Matthew did this and ended up with three stents to his left anterior descending. His slow start was due to skepticism that the program worked and just plain forgetfulness.

· Extreme stress--One of our earliest failures was a 38-year old man whose heart scan score doubled in one year, despite doing everything right. But three family members, all close to him, died within the space of six months, including his mother and a brother. I regard this as one of those instances in which we were powerless, unfortunately, though it is a graphic example of the power of unresolved stress and grief.

· Having a “better way”--These are the couple of people who were convinced that they had a better way to control their heart scan score. David firmly believed that his two dozen supplements and exercise program would drop his score. Instead, they permitted a 42% increase. Lee relied exclusively on chelation, along with several supplements of his own design. Lee had three-vessel bypass surgery.

· Starting too late--Gerome started with a score of 1179, but also was having chest pressure with emotional stress. His stress test was abnormal, with the entire upper half of his heart not receiving blood with exercise on a stress nuclear study (“anterior ischemia”). Gerome received four bypass grafts. Unfortunately, Gerome never really had a chance to engage in the Track Your Plaque program, since his health and safety were in jeopardy as soon as he started.

Have we had any big failures of people who did everything right, were compliant, were not subject to extreme stress (more than just job stress, or financial worries), didn’t neglect the basic requirements of the Track Your Plaque program, and had sufficient time (at least 6 months to 1 year)? No, thankfully, we have not.

No one who has stuck to the program has had a big failure.

Be smarter than your cardiologist

“Do you need a stent?”

Sad to say, but that sentence condenses the wisdom of over 90% of practicing cardiologists.

Prevention of heart disease means take Lipitor or some other statin and cutting the saturated fat in your diet. That’s it. Maybe throw in exercise.

Regression of coronary plaque? That phrase has only entered the conversation since the AstraZeneca-supported trial of Crestor succeeded in achieving 8% regression of plaque (Track Your Plaque Members: See News) as demonstrated by intracoronary ultrasound.



In other words, in the minds of my colleagues, it can’t be true until a drug company tells them it’s true. It’s beyond me why this brainwashing of otherwise intelligent people has occurred, but it is blatantly evident in practice.

Fish oil is another example. The spectacular benefits of fish oil have been known for 20 years. But only recently has it become a “mainstream” practice to recommend fish oil, largely because a drug manufacturer has put a preparation through the rigors of FDA approval (Omacor) and is now marketing directly to physicians. All of a sudden, fish oil is a good thing? No, it’s just achieved legitimacy in the eyes of practitioners because it graces marketing literature.

If you’re reading this, you’re likely interested in coronary plaque regression using the only tool available for you to measure, track, and regress coronary plaque: CT heart scans. Intracoronary ultrasound will achieve the same goal, but it is an invasive procedure performed at heart catheterization, involves threading a wire and imaging probe all the way down the artery, involves real risk of tearing the inner lining of the artery, and is costly (around $14,000-$20,000 for the entire package). Do it every year? That’d be nuts.

If you’re thinking about coronary plaque regression, using fish oil, concerned about patterns like low HDL and small LDL, aware of the vitamin D deficiency issue as a coronary risk factor, etc., you are far more aware than the vast majority of practicing cardiologists. They are interested in what new brand of anti-coagulant to use during their heart catheterization (because the product representative gushes about the new agent—only $1200 a dose!). Or, they are interested in gaining the procedural skills to put in a new device like a biventricular pacemaker. Regress/reverse coronary plaque? What for?

You already know that a conversation about coronary plaque reversal will not be obtained in your cardiologist’s office. Your family practice doctor or internist? Fat chance! Knee arthritis, pap smears, pneumovax inoculations, sore throats, gout, back pain—they’re spread far too thin to know anything more than the most superficial amount about coronary plaque control. Most know nothing.

That’s where we come in. That’s our mission: Educate people about the extraordinary tools that you have available to you, all in the cause of control or reversal of coronary plaque.

Why am I here?

Frank came to the office for an opinion, sent by his (proactive) family physician.

"I really don't know why I'm here, to be honest."

Two years earlier, Frank had a heart attack, survived and received two stents to his circumflex coronary artery. He now took Zocor and his LDL cholesterol was a reasonably favorable 89 mg, total cholesterol 183 mg.

"I walk with my wife every other day. I've been avoiding fish fries. You'll never see me eat fast food."

Frank was correct: If we were going to engage in the conventional approach to coronary disease, Frank was on the right track. We would have postponed his next heart attack or procedure by a couple of years. Stroke, aneurysm, and other atherosclerotic manifestations would be set back, likewise, a few years.

Would Frank have profound control over his disease? Absolutely not. In fact, his disease had probably advanced a huge amount just in the two years since his stents were placed and he was on his "prevention" program. Without his current effort, his coronary plaque would be expected to grow 30% per year. On Zocor and his modest lifestyle efforts, plaque growth was probably in the 14-28% per year range.

So I explained the unique Track Your Plaque approach to Frank. First, we start with a CT heart scan to establish where he was starting. Although he had two stents in his circumflex artery, we still had two other arteries (LAD, right coronary) to score and track.

We then attempt to identify all hidden causes of his heart disease and then correct them.

Of course, Frank had multiple hidden causes:

--HDL too low at 38 mg/dl
--Small LDL-severe, in fact, with 95% of all LDL particles in the small category
--Triglycerides too high
--Excesses of several triglyceride-containing particles (VLDL, IDL)
--Pre-diabetes--Frank had both a borderline high blood sugar and a high insulin level. This is a sure-fire stimulus to coronary plaque growth.
--A severe deficiency of vitamin D (<20 ng/ml)
--An excessivelyhigh blood pressure during exercise--With a blood pressure of 190/102 on the treadmill.

There were others(!), but that was the bulk of the causes behind Frank's coronary disease.

Once Frank recognized that there was indeed a huge panel of hidden causes for heart disease, not just too much fat in his diet and LDL cholesterol, he jumped into the program head first.

The message: The conventional approach is absurdly oversimplified, a certain path to failure for the majority of people. Even if you don't have known coronary disease like Frank, but just have a heart scan score >zero, the same principles apply to you.

Catheterization to “define coronary anatomy”

Gary is an avid jogger. On an average day, he runs 5-6 miles at a good clip. On two occasions recently, however, Gary experienced an ache in his left shoulder at mile 4. It was a toothache-like feeling, but he kept on going without difficulty.

Gary also had a heart scan score of 370.

Upon hearing of Gary’s score and his shoulder sensation, the cardiologist who saw him advised a heart catheterization “to define coronary anatomy”. (This is a real incident.)


What exactly does that mean? Why would Gary’s cardiologist need to define it?

In my view, this is an absurd notion. No one needs to “define coronary anatomy”. This catch-all phrase is commonly used to justify heart procedures. I believe what the cardiologist is saying is that it’s the easiest (for the cardiologist) and perhaps most generously reimbursed method to determine whether Gary’s symptoms are warning of an impending heart attack or not.

The problem is that the question can also be answered quite well by doing a stress test. Though not perfect diagnostic tests, stress tests are useful when symptoms are present that are doubtful in nature. Gary’s left shoulder ache could have been related to his heart, but the likelihood was that it was not. A stress test would have answered the diagnostic question quite adequately.

Instead, this man was subjected to an invasive test that was likely unnecessary. This happens dozens, if not hundreds, of times per day just around here. Nationwide, it is an epidemic of malpractice.

There are, indeed, times when a person should proceed directly to a heart catheterization. This is commonly and appropriately performed when a person develops unstable heart symptoms, such as chest discomfort or breathlessness at rest while not doing anything physical, or if the frequency is increasing, or if a stress test shows an important abnormality. There is no question that heart procedures can be lifesaving at times.

The problem is that thousands of people every year are scared into these procedures inappropriately. Beware!

It doesn't matter what I eat!

"How are your food choices?" I asked.

"What does it matter, doc? I take Lipitor. Doesn't that take care of it? I eat what I want!"

So declared Matthew. What he "wanted" was pretty much the diet of a teenager: pizza, cheeseburgers, soft drinks, snacks. His "beer belly" (visceral fat) gave it away. So did his blood work that showed flagrant lipoprotein abnormalities--small LDL, an HDL of 37 mg, and a severe after-eating flood of fat represented by increased "intermediate-density lipoprotein" (IDL).

Like many people, Matthew had been persuaded (or chose to believe) that LDL cholesterol was the sole cause for heart disease. Lipitor was therefore was all he needed. It must be great--how else could they afford all those slick TV commercials?

Well, it is definitely not true. In fact, with the persistence of Matthew's abnormal lipoprotein patterns, we should expect his heart scan score to continue to grow by 30%--the very same rate of increase as if he were taking nothing.

Specifically, Lipitor and drugs like it do not:

--Raise HDL.

--Correct or reduce the proportion of small LDL.

--Block after-eating flood of fat, nor do they accelerate clearance of unhealthy fats persisting in the bloodstream after eating.


Yes, what you eat does have real consequences, even if you take a statin drugs. In fact, the foods you ingest have a remarkably rapid and dramatic effect on what your blood contains. Any diabetic who checks his/her blood sugar knows this. They eat a slice of whole wheat toast and watch their blood sugar skyrocket.

Mind what you eat. Make it enjoyable, of course. But drugs do not provide impunity.

People with higher scores need to try harder

Sam is a 69-year retired physician. He was thoroughly enjoying retirement: golf, travelling, going out to dinner two or three times a week, spending weekends with his grandchildren. His lifestyle tended towards overindulgence, but he managed to stay fit and trim. At 6 ft 1 inch, he weighed 194 lbs and could still run 3 miles without too much difficulty. Not as good as his marathon-running days, but still not too bad for 69.

Sam's heart scan score in 2003 was a concerning 1983--extensive plaque. His doctor wasn't much help in interpreting the scan and so Sam simply chose to ignore it.

A chance conversation with a physician friend 18 months later made Sam think that perhaps this shouldn't be ignored. That's when he came to my office.




I find that sometimes the best way to motivate someone to take action is to demonstrate just how fast plaque grows if action isn't taken. So I advised Sam to get another scan first, since 18 months had passed. His score: 2441, or a 23% increase.




Sam was now starting to catch on. We made several changes in his prevention program (starting from virtually nothing). He did undergo a stress nuclear (thallium type) of test, which he passed without difficulty--normal blood flow in all heart territories despite the extensive plaque.

But, for some reason, Sam simply allowed himself to drift back to old habits: poor choices in food, overindulging in hard liquor, missing his fish oil and other supplements, and his medication, sometimes up to several days a week.

Sam started having unusual feelings in his chest. He described a sort of nervousness along with skipped heart beats. So we repeated a stress test. This time, a large area of reduced blood flow in the front of his heart ("anterior left ventricle") was detected. Sam ended up receiving three stents in a difficult procedure.

The moral: If you're starting out with a lower heart scan score of, say, 100 or 200, maybe you'll get by without trying too hard--maybe. But if your score is higher, say, several hundred or in the thousands, you got to try harder.

You're starting later in the process. Your disease will allow you very little slack. Let your guard down and it will get you. Control over your plaque is, indeed, very possible--we do it all the time. Score reduction is also possible. But your effort must be more serious and consistent.

Money can't buy health

Fallen Enron CEO, Kenneth Lay, was pronounced dead early this a.m. after suffering a heart attack.

Mr. Lay apparently had no history of heart disease and there's been no indication that symptoms provided any warning. His death was therefore classified as "sudden cardiac death".


Yet here's a man previously worth hundreds of millions of dollars with access to any test or medical system he desired--many times over. Even more recently, with his wealth reduced following his legal troubles, he and his wife managed to put away $4 million dollars to ensure an income from the interest through annuities, untouchable by the courts.

Detecting Mr. Lay's heart disease would have cost him around a few hundred dollars or whatever it costs for a CT heart scan in his city. This would have alerted his (hopefully knowledgeable) doctor that he was a time-bomb. Pile on all the stress he'd been suffering, whether deserved or no, and the diagnosis would have required little thought.

Instead, Mr. Lay has joined the thousands of Americans who will die this year because of failing to get a simple, 30-second test that costs one-tenth the cost of a stress test. Mr. Lay wasn't as lucky as former President Bill Clinton, whose doctors likewise blundered their way through and missed obvious levels of heart disease.

All Mr. Lay needed was better information: get a heart scan, then follow a program of prevention like the Track Your Plaque program. You may not have hundreds of millions of dollars, but you have the information on how to not follow in Ken Lay's footsteps. Track Your Plaque--and stay alive.

What's important, what's not in your plaque-control program

Sometimes it's hard to know what is really important in your plaque-control or plaque-reducing efforts.

There are, indeed, crucial make-it-or-break-it factors that are necessary to gain control over plaque. If you hope to stack the odds of reducing your heart scan score as much as possible in your favor, then fish oil, vitamin D, 60-60-60 in the way of standard lipids, elimination of small LDL, etc. -- all the elements of the Track Your Plaque program--are necessary.

But there's lots of things that sidetrack people. I spend much of my day fielding questions from patients about all the things that either provide very little benefit for plaque control, or provide none at all.

Among the things that we have found to be too weak or useless for plaque control, or are "non-issues", include:

--Caffeine--Go ahead and enjoy a couple cups a day (though not a pot). The effect is too trivial to make much difference.

--Hawthorne--Yes, it may dilate coronary arteries modestly, but not enough to make any difference.

--Garlic--with the possible exception of a specific preparation called Aged Garlic Extract (an acqueous, non-oil-based, extract from Kyolic), garlic's effects are too tiny to help, e.g., drop in blood pressure 1-2 points. Use it, but don't expect much. Aged Garlic Extract may be an exception, in that a single study from UCLA suggested specific effects on slowing coronary plaque growth. We await more info on this.

--Anti-oxidants--There is no shortage of extravagant claims about the benefits of anti-oxidants. Unfortunately, there's very little human exerience with pine bark extract, pycnogenol, grapeseed extract, and so on. Is the purported benefit from anti-oxidation or through some other means, e.g., enhancement of nitric oxide synthase? No data.

--Policosanol--If you've followed the Track Your Plaque Special Reports, you already know what a disappointment this agent has been, despite the too-good-to-be-true clinical data. It doesn't work.

--"No-flush niacin"--Unfortunately, no flush, no effect. This high-priced supplement is still sold widely in the U.S. despite its complete lack of efficacy. It does not work in humans. (It works great in rats!)

Track Your Plaque continues to try to be the arbiter of truth in what works, what doesn't in truly stopping or reversing your coronary plaque. The proof positive? Stopping or dropping your heart scan score.
All posts by william-davis

Medicine ain't what it used to be

The practice of medicine ain't what it used to be.

For instance:

White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.

Normal cholesterol panel . . . no heart disease?

I often hear this comment: "I have a normal cholesterol panel. So I have low risk for heart disease, right?"

While there's a germ of truth in the statement, there are many exceptions. Having "normal" cholesterol values is far from a guarantee that you won't drop over at your daughter's wedding or find yourself lying on a gurney at your nearest profit-center-for-health, aka hospital, heading for the cath lab.

Statistically, large populations do indeed show fewer heart attacks at the lower end of the curve for low total and  LDL cholesterol and the higher end of HDL. But that's on a population basis. When applied to a specific individual, population observations can fall apart. Heart attack can occur at the low risk end of the curve; no heart attack can occur at the high risk end of the curve.

First of all, to me a "normal" lipid panel is not adhering to the lax notion of "normal" specified in the lab's "reference range" drawn from population observations. Most labs, for instance, specify that an HDL cholesterol of 40 mg/dl or more and triglycerides of 150 mg/dl or less are in the normal ranges. However, heart disease can readily occur with normal values of, say, an HDL of 48 mg/dl and triglycerides of 125 mg/dl, both of which allow substantial small oxidation-prone LDL particles to develop. So "normal" may not be ideal or desirable. Look at any study comparing people with heart disease vs. those without, for instance: Typical HDLs in people with heart attacks are around 46 mg/dl, while HDLs in people without heart attacks typically average 48 mg/dl--there is nearly perfect overlap in the distribution curves.

There are also causes for heart disease that are not revealed by the lipid values. Lipoprotein(a), or Lp(a), is among the most important exceptions: You can have a heart attack, stroke, three stents or bypass surgery at age 40 even with spectacular lipid values if you have this genetically-determined condition. And it's not rare, since 11% of the population express it. How about people with the apo E2 genetic variation? These people tend to have normal fasting cholesterol values (if they have only one copy of E2, not two) but have extravagant abnormalities after they eat that contribute to risk. You won't know this from a standard cholesterol panel.

Vitamin D deficiency can be suggested by low HDL and omega-3 fatty acid deficiency suggested by higher triglycerides, but deficiencies of both can exist in severe degrees even with reasonably favorable ranges for both lipid values. Despite the recent inane comments by the Institute of Medicine committee, from what I've witnessed from replacing vitamin D to achieve serum 25-hydroxy vitamin D levels of 60-70 ng/ml, vitamin D deficiency is among the most powerful and correctable causes of heart disease I've ever seen. And, while greater quantities of omega-3 fatty acids from fish oil are associated with lower triglycerides, they are even better at reducing postprandial phenomena, i.e., the after-eating flood of lipoproteins like VLDL and chylomicron remnants, that underlie formation of much atherosclerotic plaque--but not revealed by fasting lipids.

I view standard cholesterol panels as the 1963 version of heart disease prediction. We've come a long way since then and we now have far better tools for prediction of heart attack. Yet the majority of physicians and the public still follow the outdated notion that a cholesterol panel is sufficient to predict your heart's future. Nostalgic, quaint perhaps, but as outdated as transistor radios and prime time acts on the Ed Sullivan show.

 

Idiot farm

The notion of genetic modification of foods and livestock is a contentious issue. The purposeful insertion or deletion of a gene into a plant or animal's genome to yield specific traits, such as herbicide resistance, nutritional composition, or size, prompted the Codex Alimentarius Commission, an international effort to regulate the safety of foods, to issue guidelines concerning genetically-modified foods.

The committee is aware of the concept of unintended effects, i.e., effects that were not part of the original gene insertion or deletion design. In their report, last updated in 2009, they state that:

Unintended effects can result from the random insertion of DNA sequences into the plant genome, which may cause disruption or silencing of existing genes, activation of silent genes, or modifications in the expression of existing genes. Unintended effects may also result in the formation of new or changed patterns of metabolites. For example, the expression of enzymes at high levels may give rise to secondary biochemical effects or changes in the regulation of metabolic pathways and/or altered levels of metabolites.

They make the point that food crops generated using techniques without genetic modification are released into the food supply without safety testing:

New varieties of corn, soybean, potatoes and other common food plants are evaluated by breeders for agronomic and phenotypic characteristics, but generally, foods derived from such new plant varieties are not subjected to the rigorous and extensive food safety testing procedures, including studies in animals, that are typical of chemicals, such as food additives or pesticide residues, that may be present in food.

In other words, conventional plant breeding techniques, such as hybridization, backcrossing, and introgression, practices that include crossing parental plants with their progeny over and over again or crossing a plant with an unrelated plant, yield unique plants that are not subject to any regulation. This means that unintended effects that arise are often not identified or tested. Plant geneticists know that, when one plant is crossed with another, approximately 5% of the genes in the offspring are unique to that plant and not present in either parent. It means that offspring may express new characteristics, such as unique gliadin or gluten proteins in wheat, not expressed in either parent and with new immunological potential in consuming humans.

Dr. James Maryanski, the FDA's Biotechnology Coordinator, stated during Congressional testimony in 1999 that:

The new gene splicing techniques are being used to achieve many of the same goals and improvements that plant breeders have sought through conventional methods. Today's techniques are different from their predecessors in two significant ways. First, they can be used with greater precision and allow for more complete characterization and, therefore, greater predictability about the qualities of the new variety. These techniques give scientists the ability to isolate genes and to introduce new traits into foods without simultaneously introducing many other undesirable traits, as may occur with traditional breeding. [Emphasis mine.]

Efforts by the Codex Alimentarius and FDA are meant to control the introduction and specify safety testing procedures for genetically modified foods. But both organizations have publicly stated that there is another larger problem that has not been addressed that predates genetic modification. In other words, conventional methods like hybridization techniques, the crossing of different strains of a crop or crossing two dissimilar plants (e.g., wheat with a wild grass) have been practiced for decades before genetic modification became possible. And it is still going on.

In other words, the potential hazards of hybridization, often taken to extremes, have essentially been ignored. Hybridized plants are introduced into the food supply with no question of human safety. While hybridization can yield what appear to be benign foods, such as the tangelo, a hybrid of tangerines and grapefruit, it can also yield plants containing extensive unintended effects. It means that unique immunological sequences can be generated. It might be a unique gliadin sequence in wheat or a unique lectin sequence in beans. None are tested prior to selling to humans. So the world frets over the potential dangers of genetic modification while, all along, the much larger hazard of hybridization techniques have been--and still are--going on.

Imagine we applied the hybridization techniques applied by plant geneticists to humans, mating an uncle with his niece, then having the uncle mate again with the offspring, repeating it over and over until some trait was fully expressed. Such extensive inbreeding was practiced in the 19th century German village of Dilsberg, what Mark Twain described as "a thriving and diligent idiot factory."

Eat triglycerides

Dietary fats, from olive oil to cocoa butter to beef tallow, are made of triglycerides.

Triglycerides are simply three ("tri-") fatty acids attached to a glycerol backbone. Glycerol is a simple 3-carbon molecule that readily binds fatty acids. Fatty acids, of course, can be saturated, polyunsaturated, and monounsaturated.

Once ingested, the action of the pancreatic enzyme, pancreatic lipase, along with bile acids secreted by the gallbladder, remove triglycerides from glycerol. Triglycerides pass through the intestinal wall and are "repackaged" into large complex triglyceride-rich (about 90% triglycerides) molecules called chylomicrons, which then pass into the lymphatic system, then to the bloodstream. The liver takes up chylomicrons, removes triglycerides which are then repackaged into triglyceride-rich very low-density lipoproteins (VLDL).

So eating triglycerides increases blood levels of triglycerides, repackaged as chylomicrons and VLDL.

Many physicians are frightened of dietary triglycerides, i.e, fats, for fear it will increase blood levels of triglycerides. It's true: Consuming triglycerides does indeed increase blood levels of triglycerides--but only a little bit. Following a fat-rich meal of, say, a 3-egg omelet with 2 tablespoons of olive oil and 2 oz whole milk mozzarella cheese (total 55 grams triglycerides), blood triglycerides will increase modestly. A typical response would be an increase from 60 mg/dl to 80 mg/dl--an increase, but quite small.

Counterintuitively, it's the foods that convert to triglycerides in the liver that send triglycerides up, not 20 mg/dl, but 200, 400, or 1000 mg/dl or more. What foods convert to triglycerides in the liver? Carbohydrates.

After swallowing a piece of multigrain bread, for instance, carbohydrates are released by salivary and gastric amylase, yielding glucose molecules. Glucose is rapidly absorbed through the intestinal tract and into the liver. The liver is magnificently efficient at storing carbohydrate calories by converting them to the body's principal currency of energy, triglycerides, via the process of de novo lipogenesis, the alchemy of converting glucose into triglycerides for storage. The effect is not immediate; it may require many hours for the liver to do its thing, increasing blood triglycerides many hours after the carbohydrate meal.

This explains why people who follow low-fat diets typically have high triglyceride levels--despite limited ingestion of triglycerides. When I cut my calories from fat to 10% or less--a very strict low-fat diet--my triglycerides are 350 mg/dl. When I slash my carbohydrates to 40-50 grams per day but ingest unlimited triglycerides like olive oil, raw nuts, whole milk cheese, fish oil and fish, etc., my triglycerides are 50 mg/dl.

Don't be afraid of triglycerides. But be very careful with the foods that convert to triglycerides: carbohydrates.

 

 

 

 

 

 

 

You've come a long way, baby

In 1945, the room-sized ENIAC vacuum tube computer was first turned on, women began to smoke openly in public, and a US postal stamp cost three cents. And this was the US government's advice on healthy eating:



 

 

 

 

 

 

 

 

 

 

 

 

 

Green and yellow vegetables; oranges, tomatoes, grapefruit; potatoes and other vegetables and fruits; followed by milk and milk products; meat, poultry, fish, or eggs; bread, flour, and cereals, butter and fortified margarine.

In 2011, the computing power of the ENIAC can be performed by a microchip a few millimeters in width, smoking is now banned in public places, and a first class postage stamp has increased in price by 1466%. And this is the new USDA Food Plate for Americans:



 

 

 

 

 

Have we made any progress over the past 65 years? We certainly have in computing power and awareness of the adverse effects of smoking. But have US government agencies like the USDA kept up with nutritional advice? Compare the 2011 Food Plate with the dietary advice of 1945.

It looks to me like the USDA has not only failed to keep up with the evolution of nutritional thought, but has regressed to something close to advising Americans to go out and buy stocks on the eve of the 1929 depression. Most of us discuss issues like the genetic distortions introduced into wheat, corn, and soy; the dangers of fructose; exogenous glycoxidation and lipoxidation products yielded via high-temperature cooking; organic, free-range meats and the dangers of factory farming, etc. None of this, of course, fits the agenda of the USDA.

My advice: The USDA should stay out of the business of offering nutritional advice. They are very bad at it. They also have too many hidden motives to be a reliable source of unbiased information.

 

 

Fasting with green tea

I've been playing around with brief (18-24 hour) fasts with the use of green tea. Of the several variations on fasting, such as juice "fasts,"  I've been most impressed with the green tea experience.

While the weight loss effects of daily green tea consumption are modest, there seems to be a specific satiety effect that has now been demonstrated in multiple studies, such as this and this. In other words, green tea, through an uncertain mechanism, reduces hunger. The effect is not just due to volume, since the effect cannot be reproduced with hot water alone.

I therefore wondered whether green tea might be a useful beverage to consume during a fast, as it might take the "edge" off of hunger. While hunger during a fast in the wheat-free is far less than wheat-consuming humans, there is indeed an occasional twinge of hunger felt.

So I tried it, brewing a fresh 6-8 oz cup evert two hours or so. I brewed a pot in the morning while at home, followed by brewing single cups using my tea infuser at the office. Whenever I began to experience a hunger pang, I brewed another cup and sipped it. I was pleasantly surprised that hunger was considerably reduced. I sailed through my last 18 hours, for instance, effortlessly. The process was actually quite pleasant.

I brew loose Chinese bancha, sencha, and chunmee teas and Japanese gyokuro tea. Gyokuro is my favorite, but also the most expensive. Bancha is more affordable and I've used that most frequently.

If anyone else gives this a try, please report back your experience.

Dreamfields pasta is wheat

An active question on the blogosphere and elsewhere is whether Dreamfields pasta is truly low-carb. Dr. Andreas Eenfeldt of Diet Doctor detailed his high blood glucose experience with it. Jimmy Moore of Livin' La Vida Low Carb had a similar experience, observing virtually no difference when compared to conventional pasta.

The Dreamfields people make the claim that "Dreamfields' patent-pending recipe and manufacturing process protects all but 5 grams of the carbohydrates per serving from being digested and therefore lessens post-meal blood glucose rise as compared to traditional pasta." They call the modified carbohydrates "protected" carbs.



In other words, they are making the claim that they've somehow modified the amylopectin A and amylose molecules in durum wheat flour to inhibit conversion to glucose.

I'd like to add something to the conversation: Dreamfields pasta is wheat. It is a graphic demonstration that, no matter how you cut it, press it, sauce it up, "protect" it, it's all the same thing: wheat. (It reminds me of a bad girlfriend I had in my 20s: She'd put on makeup, a pretty dress, I'd take her out someplace nice . . . She was still an annoying person who whined about everything.)

Wheat is more than a carbohydrate. It is also a collection of over 1000 proteins, including gliadins, glutens, and glutenins. Gliadins, for instance, are degraded to polypeptide exorphins that underlie the addictive potential of wheat, as well as its withdrawal phenomenon on halting consumption. Gliadin-derived exorphins are also the triggers of auditory hallucinations and paranoid delusions in schizophrenia, as well as behavioral outbursts in children with ADHD and autism.

Wheat is a source of lectins that have the curious effect of "unlocking" the proteins of the intestinal lining, the oddly-named "zonulin" proteins, that protect you from ingested foreign molecules. Ingest wheat lectins and all manner of foreign molecules gain entry into your bloodstream. Cholera works by a similar mechanism. (How about a love story: Bread in the time of cholera?)

Glutens, of course, are responsible for triggering celiac disease, the devastating small intestinal disease that now afflicts 3 million Americans, although 2.7 million don't even know it. Glutens are also responsible for neurologic conditions like cerebellar ataxia, peripheral neuropathy, and dementia ("gluten encephalopathy") and the skin condition, dermatitis herpetiformis.

Then there are the conditions for which the active wheat components have not been identified, including acid reflux, irritable bowel syndrome, asthma (excepting "bakers' asthma), rheumatoid arthritis, edema and fluid retention, and a long list of skin conditions from alopecia to gangrene.

My point: Yeah, Dreamfields pastas, from these instructive experiences, acts a lot like conventional durum wheat pasta. But, even if Dreamfields or somebody else perfects the low-carb aspect of it, it's still wheat. Modern wheat is the genetically tarted-up version of Triticum aestivum, the product of genetic shenanigans from the 1960s and 1970s.

Bet you can't fast

People who continue to consume the world's most destructive grain, i.e., wheat, can rarely endure fasting--not eating for an extended period--except by mustering up monumental willpower. That's because wheat is a powerful appetite stimulant through its 2-hour cycle of exaggerated glycemia followed by a glucose low, along with its addictive exorphin effect. Wheat elimination is therefore an important first step towards allowing you to consider fasting.

Why fast? I regard fasting as among the most underappreciated and underutilized strategies for health.

In its purest form, fasting means eating nothing while maintaining hydration with water alone. (Inadequate hydration is the most common reason for failing, often experienced as nausea or lightheadedness.) You can fast for as briefly as 15 hours or as long as several weeks (though I tell people that any more than 5 days and supervision is required, as electrolyte distortions like dangerously low magnesium levels can develop).

Among its many physiological benefits, fasting can:

  • Reduce blood pressure. The blood pressure reducing effect can be so substantial that I usually have people hold some blood pressure medications, especially ACE inhibitors and ARB agents, during the fast since blood pressure will drop to normal even without the drugs. (A fascinating phenomenon all by itself.)

  • Reduce visceral fat, i.e., the fat that releases inflammatory mediators and generates resistance to insulin.

  • Reduce inflammatory measures

  • Reduce liver output of VLDL that cascades into reduced small LDL, improved HDL "architecture," and improved insulin responsiveness. (The opposite of fasting is "grazing," the ridiculous strategy advocated by many dietitians to control weight. Grazing, or eating small meals every two hours, is incredibly destructive for the opposite reason: flagrant provocation of VLDL production.)

  • Accelerate weight loss. One pound per day is typical.


Beyond this, fasting also achieves unique subjective benefits, including reduced appetite upon resumption of eating. You will find that as single boiled egg or a few slices of cucumber, for example, rapidly generate a feeling of fullness and satisfaction. Most people also experience greater appreciation of food--the sensory experience of eating is heightened and your sense of texture, flavors, sweetness, sourness, etc. are magnified.

After decades of the sense-deadening effects of processed foods--over-sugared, over-salted, reheated, dehydrated then just-add-water foods--fasting reawakens your appreciation for simple, real food. On breaking one of my fasts, I had a slice of green pepper. Despite its simplicity, it was a veritable feast of flavors and textures. Just a few more bites and I was full and satisfied.

Once you've fasted, I believe that you will see why it is often practiced as part of religious ritual. It has an almost spiritual effect.

More on fasting to come . . .

Total cholesterol 220

Talking about total cholesterol is like wearing a tie-dyed t-shirt with the peace sign emblazoned on the front: So totally 60s and out of date.

But talk of total cholesterol somehow keeps on coming back. After I spend 45 minutes discussing a patient's lipoprotein patterns, for instance, they'll asking something like, "But what's my total cholesterol?"

To help put this ridiculous notion of total cholesterol to rest, let me paint several pictures of what total cholesterol can tell you. Let's start with a theoretical, but very common, total cholesterol value of 220 mg/dl. Recall that:

LDL cholesterol = total cholesterol - HDL cholesterol - triglycerides/5

Note that LDL cholesterol is nearly always a calculated value. (Yes, your doctor has been treating a calculated, what I call "fictitious," value.)

Rearranging the equation:

Total cholesterol = LDL cholesterol + HDL cholesterol + Triglycerides/5

This relationship means that a great many variations are possible, all under total cholesterol = 220 mg/dl. For example:

LDL 95 mg/dl + HDL 105 mg/dl + Triglycerides 100 mg/dl

(a relatively low-risk pattern for heart disease)

LDL 160 mg/dl + HDL 50 mg/dl + Triglycerides 50 mg/dl

(an indeterminate risk pattern, potentially moderate risk)

LDL 120 mg/dl + HDL 30 mg/dl + Triglycerides 350 mg/dl

(a potentially high-risk pattern)

LDL 60 mg/dl + HDL 25 mg/dl + Triglycerides 675 mg/dl

(an indeterminate risk pattern)

 

That's just a sample of the incredible variation of patterns that can all fall under this simple observation, total cholesterol 220 mg/dl.

Total cholesterol is an outdated concept, one ready long ago for the junk heap of outdated ideas. It's time to throw total cholesterol out in the trash along with beliefs like high-fat intake causes diabetes, whole grains are healthy, and the tooth fairy will leave you money when you leave your molars under the pillow.

Scientists are freakin' liars

So says Tom Naughton, referring to the frequent misinterpretations or misrepresentations of data that characterize much medical research. Dr. Andreas Eenfeldt posted Tom Naughton's recent wonderfully engaging and hilarious talk from Jimmy Moore's Low-Carb Cruise on his Diet Doctor blog.

Comedian and blogger Tom Naughton, also the filmmaker of the movie Fat Head, has brought humor and personality into the low-carb movement. I told my wife to watch it and I could hear her laughing from 30 feet away while watching her laptop.

Dr. Eenfeldt is a sensation of sorts himself, making a big low-carb splash in Sweden. While I missed the cruise this year (due to time pressures), it's clear that Eenfeldt and Naughton have contributed substantially to helping people understand the nonsense that passes as dietary advice in the U.S. and the world.

I watched Naughton's talk while eating my three eggs scrambled with ricotta cheese. I almost spit my eggs out at the computer screen I was laughing so hard.